Photodynamic therapy (PDT) is a therapy employed routinely in the treatment of superficial dermatological malignancies and is under investigation for a range of additional tumour types. Most applications of PDT involve the use of an active compound, known as a photosensitizer, and a light source, the wavelength of which can be chosen to be appropriate for exciting the photosensitizer to produce reactive oxygen species. This leads to the destruction of any tissues which have either selectively taken up the photosensitizer or have been locally exposed to light.
For example, a PDT treatment of human skin cancer may involve the following steps. Firstly, a photosensitizer precursor is administered to the patient. The photosensitizer precursor is taken up by the cells and converted to a photosensitizer. The area to be treated is then exposed to light of the appropriate wavelength. The photosensitizer absorbs light and reacts with nearby tissue oxygen, resulting in reactive oxygen species. These reactive oxygen species react with biomolecules, fatally damaging some of the cells in the treatment area.
PDT has particularly found a niche in the treatment of dermatological tumours where light can be readily applied to the surface of the skin; clinically substantial subsets of skin tumours are difficult to treat by conventional therapies (because of size, site or multiple lesions presentation). In the treatment of skin conditions, the photosensitizer or photosensitizer precursor can be applied topically, and locally excited by a light source. In the local treatment of internal cancer cells, on the other hand, photosensitizers or photosensitizer precursors can for example be administered intravenously and light can be delivered to the target area using endoscopes and fibre optic catheters. Compared to normal healthy tissues, most types of cancer cells are especially active in both the uptake and accumulation of photosensitizers, which makes cancer cells especially vulnerable to PDT, since having more photosensitizer present in a cell leads to more damage to that cell during PDT.
Photosensitizer precursors currently employed in dermatological PDT include aminolevulinic acid (ALA), methyl aminolevulinate (MAL) and hexyl aminolevulinate (HAL). If ALA, MAL or HAL is used as a photosensitizer precursor, it is converted by the cells to the photosensitizer protoporphyrin IX (PpIX).

Porphyrins have long been considered as suitable agents for tumour photodiagnosis and tumour PDT because cancer cells exhibit a significantly greater uptake and affinity for porphyrins compared to normal quiescent tissues; cancer cells therefore naturally accumulate porphyrins.
An additional feature of the photosensitizer protoporphyrin IX (PpIX) is its ability to fluoresce, which in combination with cancer cells' natural accumulation of porphyrins allows for photodiagnosis (PD) of tumours. PD has been used by surgeons for enabling greater precision in the removal of tumours, such as for example brain tumours.
PpIX is naturally present in all nucleated mammalian cells at low concentrations; it is an intermediate in the biosynthesis of haem. In the haem biosynthesis, ALA is converted to PpIX (via a number of intermediate steps), after which PpIX is converted to haem by the insertion of a Fe2+ ion into PpIX by the enzyme ferrochelatase.
In order for PDT to be effective, it is necessary to increase the amount of PpIX which is present in a cell. One way of doing this is to add more ALA, MAL or HAL to a cell, which will be converted to PpIX. However, the haem biosynthesis pathway has a maximum limit over which additional precursor administration does not produce any additional benefit. Furthermore, excessive ALA oral administration has been demonstrated to induce liver toxicity in humans. Usually, the presence of free haem acts as a negative feedback mechanism inhibiting ALA synthesis. However, the exogenous administration of large amounts of ALA or MAL bypasses this negative feedback signal and results in a temporary accumulation of PpIX within the cells, since the insertion of Fe2+ into PpIX to form haem is relatively slow. Furthermore, PpIX may accumulate in the cell even more by slowing down the step of converting PpIX to haem by insertion of Fe2+, which may be achieved by limiting the iron supply in a cell. Bech, O. et al., J Photochem Photobiol B, 1997, 41, 136-144; Curnow, A. et al., BJC, 1998, 78, 1278-1282; Pye, A. et al., Photochem Photobiol, 2007, 83(3), 766-73; and Blake, E. et al., Photochem Photobiol, 2010, 86(5), 1154-60 describe how the use of the iron chelator CP94, shown below, in combination with ALA can increase accumulation of PpIX.

A need however remains for new photosensitizer precursors which have an improved activity profile in photodynamic therapy, especially since currently photodynamic therapy is not effective for all tumour types; clearance rates for thicker nodular basal cell carcinoma (BCC), for example, remain lower than for superficial BCC.
It is an aim of the invention to provide a new compound which can be used as a photosensitizer precursor, and which can show an improved activity profile in photodynamic therapy.